Evidence suggests that exposure to ambient air particles promotes altered autonomic nervous system function, systemic inflammation, and vascular endothelial injury and dysfunction. Although epidemiologic Studies suggest that people older than 65 years are at greatest risk of pollution-related cardiovascular events, these mechanistic hypotheses have frequently been evaluated in young healthy volunteers or specific patient populations, rather than in unselected community-dwelling elderly. Accordingly, we will conduct a prospective, repeated-measures study to evaluate the mechanisms by which particulate air pollution affects autonomic function, inflammation, and vascular endothelial injury and function in a cohort of community dwelling elderly aged 65 years or older. Specifically, we will link detailed environmental data with non-invasive measures of autonomic nervous system function (heart rate variability), systemic inflammation (circulating levels of specific serum markers), and endothelial function (cerebral vascular resistance and reactivity). We will assess short-term exposure to ambient air pollution using prospectively-collected measurements from a central ambient monitoring site. Available environmental data includes hourly measures of fine particulate matter (PM2.5), black carbon (BC, a measure of traffic-related pollution), sulfates (a measure of regional pollution), gaseous pollutants (CO, N02, S02, ozone), and meteorologic data. Additionally, we will use a validated spafiotemporal land-use regression model to predict short-term residential exposure to pollution specifically from traffic. We hypothesize that short-term exposure to ambient PM will be associated with adverse changes in autonomic function, inflammation, and vascular function. Results supporting these hypotheses would suggest that ambient PM has adverse effects in a representative population-based sample of community-dwelling elderly and provide insight into the mechanism of pollution-related acute cardiovascular events.